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• We examined the treatment of 338 patients with nonbipolar major depressive disorders during the first eight weeks after entry into the National Institute of Mental Health—Clinical Research Branch Collaborative Program on the Psychobiology of Depression: Clinical Study. Of the 250 entered as inpatients, 31% received either no antidepressant somatotherapy or very low or unsustained levels, and only 49% received at least 200 mg of imipramine hydrochloride (or its equivalent) for four consecutive weeks. Of these patients, 19% received less than 30 minutes of psychotherapy per week. Among the 88 who entered as outpatients, 29% received no antidepressant somatotherapy; another 24% received very low or unsustained levels; only 19% received at least 200 mg of imipramine hydrochloride or its equivalent for four consecutive weeks. Of these patients, 52% received less than 30 minutes of psychotherapy per week. Only a few clinical factors were found to be predictive of treatment intensity. Very large differences in the amount and type of treatment across the five collaborating university centers do not appear to be related to differences in patient characteristics.

• As part of the National Institute of Mental Health—Clinical Research Branch Collaborative Program on the Psychobiology of Depression Clinical Study, 2,289 relatives of 523 probands with affective disorder were interviewed with the Schedule for Affective Disorders and Schizophrenia and diagnosed for major depressive disorder by the Research Diagnostic Criteria. Data were analyzed using life-table and survival methods. The findings suggest a progressive increase in rates of depression in successive birth cohorts through the 20th century and an earlier age at onset of depression in each birth cohort. A predominance of female depressives was found in all birth cohorts but the magnitude of female-male differences fluctuated over the decades. The existence of these trends is reported to stimulate further research. These findings are discussed in terms of possible gene-environment interactions. However, no conclusive causal inferences can be drawn pending further investigation.

• As part of the National Institute of Mental Health Collaborative Program on the Psychobiology of Depression study, data were collected on 2225 first-degree relatives of 612 probands. We analyzed 187 families of bipolar patients (149 probands with a diagnosis of bipolar I disorder and 38 with a diagnosis of schizoaffective, manic subtype). Using traditional genetic methods, the morbid risk of bipolar illness in relatives was found to be 5.7% in the relatives of bipolar probands as contrasted with 1.1% in the relatives of probands with major depression. These values compared closely with those obtained using survival analysis. Relatives of probands with early onset were found to have a greater risk than relatives of probands with late onset. The sex of the relative, the sex of the proband, or the subtype of the proband (bipolar I or schizoaffective bipolar) did not influence the risk in the relative. The age at onset was found to be accelerated with birth cohort, with individuals born in more recent cohorts having an earlier onset. Multifactorial analysis found significant heterogeneity for sex-specific sibling correlations (with the brother-sister correlation smaller than the same-sexed correlations), and path analysis estimated transmissibility of liability to be 71%. The mixed model, which allows for a single major locus with a multifactorial background, gave evidence for the presence of a major locus when controlling for the effects of birth cohort and age at onset. However, this evidence is tempered when comparing the mixed model with a more general transmission model.

• We examined familial rates of affective disorder and related illness in a cohort of 955 probands studied at five centers in the National Institute of Mental Health Collaborative Study of the Psychobiology of Depression: Boston, Chicago, Iowa City, New York, and St Louis. Six hundred sixteen of these probands were entered into a family study, and 3423 of their first-degree relatives were evaluated. The probands were divided into five diagnostic groups: schizoaffective-bipolar (n = 37), schizoaffective-depressed (n =18), bipolar I (n =151), bipolar II (n = 76), and unipolar (n = 330). The relatives of bipolar I probands had a higher rate of bipolar I illness than the relatives of unipolar probands, but the relatives of unipolar probands did not have a higher rate of unipolar illness than the relatives of bipolar I probands. The relatives of probands with schizoaffective disorder, depressed subtype, had a higher rate of schizophrenia than the relatives of schizoaffective-bipolar probands, suggesting that bipolar schizoaffective disorder may be closer to pure affective disorder while schizoaffective depression may be closer to schizophrenia. An increase in bipolar II illness was also observed in the relatives of bipolar II probands. Overall, these data support the widely accepted distinction between bipolar and unipolar affective disorders.

IN REPLY Lurie and Geyer question our finding that shared environment did not contribute to susceptibility to posttraumatic stress disorder symptoms in our study of 2224 MZ and 1818 DZ male veteran twins. 1 They base their argument on the validity of the equal environments assumption of twin studies, which is that MZ and DZ twins do not differ in exposure to etiologically relevant environmental influences.Although, as stated in the article, we did not have data in our study to test directly this assumption, the issue has received considerable critical attention in the twin literature, most recently in Kendler' s2 comprehensive review of the role of twin studies of psychiatric illness and in a review of genetic approaches to personality by Eaves et al:3 The issue is that if the phenotypic similarity of MZ twins is actually attributed to shared environments that are more uniform, then genetic contributions will

TO THE EDITOR.— Dr Jonathan Stewart of the New York State Psychiatric Institute has brought to our attention an error that appeared in our article.1 In Table 7, there was a misprint; the P value produced when unipolar depression is defined as need for hospitalization should have been.0931 rather than.0031. In addition, in that table, a colon was inadvertently inserted for a period in the typesetting process. The numbers in the last column of that table should have read 1.2, 1.4, etc, rather than 1:2, 1:4, etc. The insertion of colons erroneously gives the impression of higher unipolar-bipolar ratios than actually exist.We appreciate having an opportunity to clarify these points.